PCGF1 promotes epigenetic activation of stemness markers and colorectal cancer stem cell enrichment

Ji, Guangyu; Zhou, Wenjuan; Du, Jikun; Zhou, Juan; Wu, Dong; Zhao, Man; Yang, Liping; Hao, Aijun

doi:10.1038/s41419-021-03914-2

Cited by 26 publications

(25 citation statements)

References 50 publications

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“…Furthermore, a variety of molecular pathways including PCGF1, circFAM73A, CXCL1 and NUMB are able to affect CSC features. The growth, metastasis and therapy response are mainly regulated by CSC characteristics [ 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 ].…”

Section: Cancer Stem Cells In Oncologymentioning

confidence: 99%

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Paskeh

Asadi²,

Zabolian

et al. 2021

IJMS

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As a multifactorial disease, treatment of cancer depends on understanding unique mechanisms involved in its progression. The cancer stem cells (CSCs) are responsible for tumor stemness and by enhancing colony formation, proliferation as well as metastasis, and these cells can also mediate resistance to therapy. Furthermore, the presence of CSCs leads to cancer recurrence and therefore their complete eradication can have immense therapeutic benefits. The present review focuses on targeting CSCs by natural products in cancer therapy. The growth and colony formation capacities of CSCs have been reported can be attenuated by the dietary agents. These compounds can induce apoptosis in CSCs and reduce tumor migration and invasion via EMT inhibition. A variety of molecular pathways including STAT3, Wnt/β-catenin, Sonic Hedgehog, Gli1 and NF-κB undergo down-regulation by dietary agents in suppressing CSC features. Upon exposure to natural agents, a significant decrease occurs in levels of CSC markers including CD44, CD133, ALDH1, Oct4 and Nanog to impair cancer stemness. Furthermore, CSC suppression by dietary agents can enhance sensitivity of tumors to chemotherapy and radiotherapy. In addition to in vitro studies, as well as experiments on the different preclinical models have shown capacity of natural products in suppressing cancer stemness. Furthermore, use of nanostructures for improving therapeutic impact of dietary agents is recommended to rapidly translate preclinical findings for clinical use.

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Section: Cancer Stem Cells In Oncologymentioning

confidence: 99%

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Paskeh

Asadi²,

Zabolian

et al. 2021

IJMS

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“…Polycomb group factor 1 (PCGF1), which is also known as nervous system polycomb1 (NSPc1), was first identified in 2001 ( 13 , 14 ). PCGF1 is a novel mammalian polycomb gene, belongs to the polycomb group (PcG) protein family, and plays a significant role in the development of the nervous system ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

“…The abnormal expression of PCGF1 has been implicated in cancer stem cell phenotypes and has been shown to promote tumorigenesis in various types of cancers ( 21 , 22 ). PCGF1 was shown to be overexpressed in colorectal cancer (CRC) and was linked to cancer progression and a poor prognosis ( 14 ). In CRC, PCGF1 contributes to stem cell enrichment and induces the activation of stem cell biomarkers ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

“…PCGF1 was shown to be overexpressed in colorectal cancer (CRC) and was linked to cancer progression and a poor prognosis ( 14 ). In CRC, PCGF1 contributes to stem cell enrichment and induces the activation of stem cell biomarkers ( 14 ). Research has shown that the downregulation of PCGF1 in gliomas leads to the inactivation of the c-myc signaling pathway and reduces cell proliferation ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

“…Research has shown that the downregulation of PCGF1 in gliomas leads to the inactivation of the c-myc signaling pathway and reduces cell proliferation ( 15 ). PCGF1 expression is increased in several cancer types ( 14 ) and regulates the ability of stem cell self-renewal by targeting retinol dehydrogenase 16 (RDH16) in glioma cells ( 21 ); however, to date, no studies have explored its prognostic and diagnostic value and the regulatory network of PCGF1 in LIHC. Additionally, the expression, prognosis, and mechanism of PCGF1, and the role of tumor immune infiltration in LIHC remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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The non-coding RNA (ncRNA)-mediated high expression of polycomb group factor 1 (PCGF1) is a prognostic biomarker and is correlated with tumor immunity infiltration in liver hepatocellular carcinoma

Liu¹,

Xu²,

Sun³

et al. 2022

Ann Transl Med

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Background Liver hepatocellular carcinoma (LIHC) has a poor prognosis worldwide. Polycomb group factor 1 (PCGF1) was recently reported to play a tumor suppressive role in cancers. However, the molecular mechanism and competitive endogenous ribonucleic acid (ceRNA) regulatory networks of PCGF1 in LIHC are still unclear. Methods We constructed a PCGF1 ceRNA regulatory network in LIHC and identified potential prognostic markers, especially for tumor immunity. We identified the gene expression profiles and conducted correlation and survival analyses of PCGF1 and the related RNAs. We also explored the clinicopathological features and diagnostic and prognostic values of PCGF1 and constructed a nomogram to predict 1-, 3-, and 5-year survival. Based on a variety of bioinformatics tools, we confirmed the PCGF1-related signaling pathways in LIHC. Finally, the role of PCGF1 in immune cell infiltration was also analyzed. Results We found that PCGF1 was overexpressed in LIHC (P<0.001) and was linked to a poor prognosis in terms of overall survival (OS, P=0.029), the progress-free interval (PFI, P=0.002), and disease-free survival (DFS, P=0.02). Hsa-miR-22-3p was highly negatively correlated with PCGF1. Further, 3 upstream long non-coding RNAs (lncRNAs) (i.e., AC016405.3, BX284668.6, and MIR4435-2HG) were confirmed to further research. PCGF1 was positively associated with pathologic tumor stages (P=0.001), histologic grade (P=0.030), alpha fetoprotein (AFP) level (P=0.030), and vascular invasion (P=0.022). The area under the curve of PCGF1 was 0.983 [confidence interval (CI): 0.972–0.994]. In the multivariate analyses, high PCGF1 expression remained an independent factor associated with OS [hazards ratio (HR): 1.696, P=0.027], DSS (HR: 2.139, P=0.024), and the PFI (HR: 1.512, P=0.034). We found that PCGF1 was involved in some malignancy-associated signaling pathways and plays a role in regulating the immune response. Conclusions We confirmed the upstream ceRNA regulatory network of PCGF1 in LIHC. PCGF1 has an oncogenic effect and correlates with tumor immunity.

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UTX inhibition suppresses proliferation and promotes apoptosis in patient‐derived glioblastoma stem cells by modulating periostin expression

Luan,

Zhang,

Liu

et al. 2024

Journal Cellular Physiology

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Glioblastoma stem cells (GSCs) exert a crucial influence on glioblastoma (GBM) development, progression, resistance to therapy, and recurrence, making them an attractive target for drug discovery. UTX, a histone H3K27 demethylase, participates in regulating multiple cancer types. However, its functional role in GSCs remains insufficiently explored. This study aims to investigate the role and regulatory mechanism of UTX on GSCs. Analysis of TCGA data revealed heightened UTX expression in glioma, inversely correlating with overall survival. Inhibiting UTX suppressed GBM cell growth and induced apoptosis. Subsequently, we cultured primary GSCs from three patients, observing that UTX inhibition suppressed cell proliferation and induced apoptosis. RNA‐seq was performed to analyze the gene expression changes after silencing UTX in GSCs. The results indicated that UTX‐mediated genes were strongly correlated with GBM progression and regulatory tumor microenvironment. The transwell co‐cultured experiment showed that silencing UTX in the transwell chamber GSCs inhibited the well plate cell proliferation. Protein–protein interaction analysis revealed that periostin (POSTN) played a role in the UTX‐mediated transcriptional regulatory network. Replenishing POSTN reversed the effects of UTX inhibition on GSC proliferation and apoptosis. Our study demonstrated that UTX inhibition hindered POSTN expression by enhancing the H3K27me2/3 level, eventually resulting in inhibiting proliferation and promoting apoptosis of patient‐derived GSCs. Our findings may provide a novel and effective strategy for the treatment of GBM.

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PCGF1 promotes epigenetic activation of stemness markers and colorectal cancer stem cell enrichment

Cited by 26 publications

References 50 publications

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

The non-coding RNA (ncRNA)-mediated high expression of polycomb group factor 1 (PCGF1) is a prognostic biomarker and is correlated with tumor immunity infiltration in liver hepatocellular carcinoma

UTX inhibition suppresses proliferation and promotes apoptosis in patient‐derived glioblastoma stem cells by modulating periostin expression

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